Abstract
Homocysteine is a sulfhydryl-containing amino acid derived from the essential amino acid methionine. Total Hcy plasma level varies in the range of 5-15 μmol/L in the normal population. Our aim in this study was to investigate the possible correlations among homocysteine plasma levels, oxidative stress parameters and clinical evolution of stroke. Fifty patients with large-vessel ischemic stroke were studied. Biochemical determinations were performed at entry (T0) and then repeated one month after stroke (T1). Homocysteine levels were significantly increased at T0 with respect to T1 and showed a significant positive correlation with the expression of oxidative stress markers and a negative correlation with indicators of protective anti stress activity. A significant increase of antioxidant activity occurred from T0 to T1 and changes were associated with the severity of clinical conditions. In particular, the extent of homocysteine and of oxidative stress markers plasmatic levels re- duction and of the contemporary increase in anti stress biochemical activities were associated with a reduction of NIHSS scores. These findings, besides confirming an involvement of oxidative stress in in- fluencing the evolution of stroke, suggest a role for homocysteine as a potentially modifiable biochemical alteration able to modulate some mechanisms in- volved in the production of ischemic damage.
Highlights
In a previous study, we demonstrated that changes in some oxidative stress markers are significantly lower in patients with lacunar stroke compared to large-vessel stroke patients [12]
Homocysteine values were significantly lower after one month (T1) from ischemic attack compared to stroke onset (T0) (Figure 1)
Idiopathic ischemic stroke is an important cause of death in general population and it is emerging as a prominent health problem in developed countries [24]
Summary
*Conflict of interest: The authors declare that they have no conflict of interest. #These Authors contributed in this work. †Corresponding author. Homocysteine causes oxidative stress and vascular inflammation, damages endothelial cells, inhibits endothelium-dependent relaxation, and enhances thrombogenicity [4]. A large body of epidemiological studies suggest that increased homocysteine level may be considered as an independent risk factor for vascular diseases, including stroke [5,6,7]. Ischemic stroke is a heterogeneous syndrome caused by multiple disease mechanisms, resulting in a disruption of cerebral blood flow with subsequent tissue damage. Hyperhomocysteinemia-induced oxidative stress may occur as a result of decreased expression and/or activity of key antioxidant enzymes as well as increased enzymatic generation of superoxide anion The aim of this study was to analyze changes in homocysteine levels in ischemic stroke patients in the acute phase and after a month from disease onset. We investigated the possible correlations among homocysteine values, oxidative stress parameters and clinical evolution
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